Our broad portfolio consists of multiplex panels that allow you to choose, within the panel, analytes that best meet your needs. On a separate tab you can choose the premixed cytokine format or a single plex kit.

Cell Signaling Kits & MAPmates™

Choose fixed kits that allow you to explore entire pathways or processes. Or design your own kits by choosing single plex MAPmates™, following the provided guidelines.

The following MAPmates™ should not be plexed together:
-MAPmates™ that require a different assay buffer
-Phospho-specific and total MAPmate™ pairs, e.g. total GSK3β and GSK3β (Ser 9)
-PanTyr and site-specific MAPmates™, e.g. Phospho-EGF Receptor and phospho-STAT1 (Tyr701)
-More than 1 phospho-MAPmate™ for a single target (Akt, STAT3)
-GAPDH and β-Tubulin cannot be plexed with kits or MAPmates™ containing panTyr

MILLIPLEX MAP Mouse Isotyping Magnetic Bead Panel, measuring mouse IgG subclasses (1, 2a, 2b, 3), IgM, and IgA, has been designed to enable you to measure both classes and subclasses accurately – all in one well. In addition this panel allows you to choose only those immunoglobulins you need for your experiments.

Background Information

Produced by plasma cells and lymphocytes, immunoglobulins (antibodies) are critically involved in immune response, attaching to antigens and playing a role in their destruction. Immunoglobulins (Ig) can be classified by isotype, classes that differ in function and antigen response due to structure variability. Six major isotypes have been identified in placental mammals: IgM, IgG1, IgG2a, IgG2b, IgG3 and IgA – all found in normal individuals. Immunoglobulin-deficiency disorders, such as autoimmune disease, some GI conditions and malignancies, are characterized by specific isotype deficiencies or varying concentrations of one or more isotypes. Disease states can range from the absence of one isotype class or subclass to a total deficiency of immunoglobulin classes.

References

Product Information

Detection method

Luminex xMAP

Configuration

Design your multiplex kit by choosing available analytes within this panel.

• This kit may be used for the analysis of IgG1, IgG2a, IgG2b, IgG3, IgA and IgM in mouse serum or tissue/cell lysate and culture supernatant samples.• There are 2 one-hour room-temperature incubations.• This assay requires 50 µl of 1:50,000 diluted plasma or serum, or 50 μL cell culture supernatant diluted to approximately 1μg/mL Ig per well.

Biological Information

Specificity

Cross-reactivity between these antibodies and those against other immunoglobulins is non-detectable or negligible.

Species Reactivity

Mouse

Analytes Available

IgG1

IgG2a

IgG2b

IgG3

IgA

IgM

Accuracy

IgG1 96%

IgG2a 76%

IgG2b 98%

IgG3 85%

IgA 98%

IgM 100%

Physicochemical Information

Sensitivity

IgG1 0.7 ng/mL

IgG2a 0.67 ng/mL

IgG2b 0.18 ng/mL

IgG3 0.32 ng/mL

IgA 1.1 ng/mL

IgM 1.73 ng/mL

Standard Curve Range

IgG1: 2 – 1,500 ng/mL

IgG2a: 3 – 2,000 ng/mL

IgG2b: 1 – 900 ng/mL

IgG3: 2 – 1,500 ng/mL

IgA: 5 – 3,000 ng/mL

IgM: 2 – 1,500 ng/mL

Dimensions

Materials Information

Toxicological Information

Safety Information according to GHS

Safety Information

Product Usage Statements

Usage Statement

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

To investigate the efficacy of different doses of the soluble form of the receptor for advanced glycation end products (sRAGE) (conjugated to the Fc portion of immunoglobulin) in the treatment of nephritis in lupus-prone mice, in comparison with the efficacy of combination therapy with mycophenolate mofetil plus prednisolone.Twenty-eight female (NZB/NZW)F1 mice were divided into 5 groups (untreated, sRAGE [dose groups of 0.5, 1, or 2 μg], or mycophenolate mofetil plus prednisolone). Proteinuria and histologic damage were evaluated. Immune complex deposition and the nuclear translocation of NF-κB in the kidney tissue were assessed by immunofluorescence staining. Serum concentrations of anti-double-stranded DNA (anti-dsDNA) and IgG subclasses were also measured. The population of T cells was evaluated using a fluorescence-activated cell sorter, and expression of intracellular adhesion molecule 1 and vascular cell adhesion molecule 1 in the kidney tissue was assessed by immunohistochemical staining.In comparison with untreated mice, mice treated with 1 or 2 μg sRAGE showed significantly reduced proteinuria and attenuated histologic renal damage, with efficacy comparable to that of combination therapy. Treatment with 2 μg sRAGE significantly reduced immune complex deposition and decreased the serum concentrations of anti-dsDNA, IgG2a, IgG2b, and IgG3. In addition, sRAGE interrupted the nuclear translocation of NF-κB in the kidney, resulting in reduction in the expression of downstream genes of NF-κB in vivo and in vitro. Furthermore, sRAGE effectively modified T cell populations.Treatment with sRAGE significantly improved nephritis in lupus-prone mice, with efficacy comparable to that of standard induction treatment for lupus nephritis. These data suggest that sRAGE has antiinflammatory effects on the pathophysiology of lupus nephritis and could serve as a potent new therapy for this disease.

By inhibiting target gene expression, microRNAs (miRNAs) play major roles in various physiological and pathological processes. miR-146a, a miRNA induced upon lipopolysaccharide (LPS) stimulation and virus infection, is also highly expressed in patients with immune disorders such as rheumatoid arthritis, Sjögren's syndrome, and psoriasis. Whether the high level of miR-146a contributes to any of these pathogenesis-related processes remains unknown. To elucidate the function of miR-146a in vivo, we generated a transgenic (TG) mouse line overexpressing miR-146a. Starting at an early age, these TG mice developed spontaneous immune disorders that mimicked human autoimmune lymphoproliferative syndrome (ALPS) with distinct manifestations, including enlarged spleens and lymph nodes, inflammatory infiltration in the livers and lungs, increased levels of double-negative T cells in peripheral blood, and increased serum immunoglobulin G levels. Moreover, with the adoptive transfer approach, we found that the B-cell population was the major etiological factor and that the expression of Fas, a direct target of miR-146a, was significantly dampened in TG germinal center B cells. These results indicate that miR-146a may be involved in the pathogenesis of ALPS by targeting Fas and may therefore serve as a novel therapeutic target.